dyrk1a prolongs the kinetics of ERK activation by interacting with Ras, B-Raf, and MEK1 to facilitate the formation of a Ras/B-Raf/MEK1 multiprotein complex. Dyrk 1a is required for promoting or maintaining neuronal differentiation and its overexpression contributes to the neurological abnormalities observed in Down syndrome patients (Kelly and Rahmani, 2005). Dyrk1a regulates cell cycle exit, oncogene-induced senescence, and cell differentiation and acts as an oncogene in myeloid leukemias and gliomas (Abbassi et al., 2015; Lee et al., 2016). This evidence concerns the gene MAPK1 and myeloid leukemia.